This is how Renal compensation for metabolic acidosis works

Metabolic acidosis is a primary reduction in bicarbonate, typically with a compensatory reduction in carbon dioxide partial pressure (Pco2); pH may be markedly low or slightly subnormal. Metabolic acidosis is categorized as high or normal anion gap based on the presence or absence of unmeasured anions in serum. The condition of metabolic acidosis occurs when the body produces excessive quantities of acid or when the kidneys are not removing enough acid from the body. This condition could lead to acidemia when blood pH is lower than 7.35. Symptoms may include chest pain, palpitations, headache, altered mental status such as severe anxiety due to hypoxia, decreased visual acuity, nausea, vomiting, abdominal pain, lethargy, hyperpnea (increased depth of breathing when required to meet metabolic demand of body tissue), altered appetite and weight gain, muscle weakness, bone pain and joint pain. People can develop pH imbalances as a result of metabolic disorders or breathing problems, like severe asthma that limits respiration. The condition may exhibit deep, rapid breathing, increasing the amount of carbon dioxide exhaled, lowering the serum carbon dioxide levels.

Kidneys_joe cosgrove_renal compensantion_medicine

Image courtesy of Joshua Schwimmer at Flickr.com

And metabolic acidosis occurs when the body produces too much acid, or when the kidneys are not removing enough acid from the body due to the inability to generate sufficient bicarbonate. Renal compensation is an attempt by the kidneys to control the overall level of acidity, or pH, of blood serum. If it is too acidic or alkaline, the patient can develop health problems that will create a series of cascading reactions in the body. The metabolism and respiratory tract are involved in regulating internal pH through exchanging chemicals, excreting excess, and making sure the cells get the oxygen and nutrients they need. When the cells detect an imbalance, they respond by releasing chemicals to stabilize the body. If this is not successful, renal compensation may occur.

The kidneys are one of the lines of defense used to address acidosis or alkalosis. It can take several days for the renal compensation to kick in and stabilize the pH and the kidneys may not be able to maintain the desired value if the underlying cause of the problem is not addressed. The body regulates the acidity of the blood by four buffering mechanisms: The bicarbonate buffering system; intracellular buffering by absorption of hydrogen atoms by various molecules, including proteins, phosphates and carbonate in bone; respiratory compensation; and renal compensation. In situations where a metabolic acidosis develops rapidly and is short-lived, there is usually little time for much compensatory ventilatory response to take place.

Structures in the kidneys can determine if the blood is too alkaline or acidic, and decide which compounds to retain and which to excrete on this basis. They can change their absorption level of bicarbonate, for example, to control the level of acidity. Over the course of several days, the kidneys are able to filter the blood and restore balance. Changes in blood concentration result in the adjustment of excretion when renal functioning mass is acutely reduced

Renal compensation for a metabolic acidosis is hyperventilation to decrease the arterial carbon dioxide partial pressure. The metabolic acidosis is detected by both the peripheral and central chemoreceptors and the respiratory center is stimulated. The subsequent increase in ventilation causes a fall in arterial carbon dioxide partial pressure, which inhibits the ventilatory response. Beware when initiating ventilation in a patient with a significant acidosis, because the outcome could be fatal. The chemoreceptor inhibition acts to limit and delay the full ventilatory response until bicarbonate shifts have stabilized across the blood brain barrier. Joe Cosgrove explains that the expected pCO2 at maximal compensation can be calculated from a simple formula. A consistent relationship between bicarbonate level and pCO2 has been found. It can be estimated from the following equation:  Expected pCO2 = 1.5 (Actual [HCO3]) + 8 mmHg

Heart Rate and Arterial pressures wave_joe cosgrove_renal compensantion_kidneys

Image courtesy of John Campbell at Flickr.com

If a patient with a severe metabolic acidosis requires intubation and controlled ventilation in the hospital, the acidosis can markedly worsen unless the hyperventilation is maintained. The ventilation should be set to mimic the compensatory hyperventilation to keep the pCO2 low. Carbon dioxide crosses cell membranes readily so intracellular pH falls rapidly also, resulting in depression of myocardial contractility, arrhythmias and a rise in intracranial pressure.

When the underlying disorder is treated, the serum pH corrects. Caution should be exercised in these patients when providing alkali for raising the pH much higher than 7.20 because an overshoot alkalosis may occur. Potassium citrate can be useful when the acidosis is accompanied by hypokalemia but should be used cautiously in the presence of renal impairment and must be avoided in the presence of hyperkalemia. Citrate salts are available in a variety of formulations, as mixtures of citric acid with sodium citrate and/or potassium citrate. Potassium citrate is useful when the acidosis is accompanied by hypokalemia but should be used cautiously in persons with renal impairment and must be avoided in those with hyperkalemia.

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